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Biomedical subjects

S D Wilson

Publications and source records attributed to S D Wilson.

At least 19 recordsLinked to original sources
PubMed1991

Zollinger-Ellison syndrome in children: a 25-year follow-up.

The influence of gastric resection on the Zollinger-Ellison syndrome (ZES) in eight children was first reported to the Central Surgical Association 26 years ago. That report showed that the three children who had less than total gastrectomy were all dead with complications of gastric acid hypersecretion, although the five children who had total gastrectomy were living and well. During the past quarter of the century, the development of effective gastric acid inhibitors has prompted a greater emphasis on medical management in the ZES. The role of the surgeon and total gastrectomy remains controversial. Follow-up of the five young patients who had total gastrectomy shows that only one patient was dead with tumor 14 years after total gastrectomy and that the remaining four patients were alive 30, 29, 28, and 27 years, respectively, after total gastrectomy. Growth and activity have been near normal. All patients have had proven metastatic islet-cell carcinoma documented at some time in the course of the disease (lymph nodes in three patients and liver metastasis in two patients). Only one of the four living patients with total gastrectomy had a normal serum gastrin level and no apparent tumor. Gastrinoma tumor growth appears to be less aggressive in children than in adults. Complete excision of gastrinomas is possible in some patients with ZES. When hypergastrinemia persists, total gastrectomy may be preferable to lifelong medical management with gastric acid inhibitors in children and young adults with ZES.

Adolescent↗
PubMed1990

Sequence and chromosomal location of the I-309 gene. Relationship to genes encoding a family of inflammatory cytokines.

We previously reported the isolation and characterization of a cDNA clone, I-309, that encodes a small secreted protein produced by activated human T lymphocytes. This protein is structurally related to a large number of recently identified proteins that are secreted upon cellular activation. In this report we describe the isolation and characterization of the gene encoding I-309. The genomic organization is essentially identical to that found in the genes encoding the structurally similar proteins TCA-3, hJE/MCP-1, and mJE, strengthening the hypothesis that these genes are evolutionarily related. The region of the I-309 gene 5' of the mRNA cap site exhibits extensive nucleotide sequence homology with the same region of the murine gene TCA-3, providing additional evidence that I-309 and TCA-3 are likely to be homologs. Finally, panels of rodent-human somatic cell hybrids were used to map the I-309 gene to human chromosome 17. In conjunction with recent mapping data from other laboratories, this result suggests the presence of a cluster of related genes on this chromosome.

Amino Acid Sequence↗
PubMed1990

Expression and characterization of TCA3: a murine inflammatory protein.

TCA3 is a cDNA originally isolated from activated T cells. Transcription of this gene has been shown to correlate with Ag-induced cellular activation of both T cells and mast cells. Based on the predicted amino acid sequence encoded by the cDNA, we previously proposed that TCA3 represents a cytokine. In this report we have used rDNA technology to express TCA3 in two mammalian cell lines. In both cases, TCA3 was expressed as a secreted molecule with an apparent molecular mass of 16 kDa. Digestion of the (rTCA3) with the enzyme N-glycanase revealed that approximately 8 kDa is caused by N-linked glycosylation. Intradermal injection of rTCA3 into mouse footpads resulted in a rapid swelling response. The sites of injection were characterized histologically by a local accumulation of neutrophils. These findings are discussed with particular attention to a family of related proteins, some of whose members also have inflammatory properties.

Animals↗
PubMed1990

Clustering of cytokine genes on mouse chromosome 11.

The presence of positionally conserved amino acid residues suggests that the mouse proteins TCA3, P500, MIP1-alpha, MIP1-beta, and JE are members of a single gene family. These proteins are activation specific and can be expressed by both myeloid and lymphoid cells. MIP1-alpha/MIP1-beta and MCAF (the putative human homologue of JE) act as chemotactic and activating agents for neutrophils and macrophages, respectively. The functions of TCA3 and P500 are unknown. We have used interspecies somatic cell hybrids and recombinant inbred mouse strains to show that the genes encoding TCA3, MIP1-alpha, MIP1-beta, and JE (provisionally termed Tca3, Mip-1a, Mip-1b, and Sigje, respectively) map as a cluster on the distal portion of mouse chromosome 11 near the Hox-2 gene complex. DNA sequence analysis indicates that the P500 and TCA3 proteins are encoded by alternative splicing products of one genomic gene. Additionally, the genes encoding TCA3 and JE are found to be strikingly similar with respect to the positions of intron-exon boundaries. Together, these data support the model that the cytokines TCA3, P500, MIP1-alpha, MIP1-beta, and JE are encoded by a single cluster of related genes. The gene encoding IL-5 (Il-5), which acts as a T cell-replacing factor, a B cell growth factor, and an eosinophil differentiation factor, is also mapped to mouse chromosome 11.Il-5 maps approximately 25 cM proximal to the Tca-3 gene and appears tightly linked to a previously described gene cluster that includes Il-3, Il-4, and Csfgm. We discuss the potential relevance of the two cytokine gene clusters described here with particular attention to specific human hematologic malignancies associated with chromosomal aberrations at corresponding locations on human chromosomes 5 and 17.

Amino Acid Sequence↗
PubMed1990

Hereditary hyperparathyroidism and multiple ossifying jaw fibromas: a clinically and genetically distinct syndrome.

A large previously reported family with hyperparathyroidism has been reinvestigated recently because of the occurrence of multiple ossifying jaw fibromas in two affected members of the third generation similar to the jaw tumors of four of five affected members of the first generation. These maxillary and mandibular tumors can be differentiated from the "brown tumors" of hyperparathyroidism because they can appear and enlarge even though the hypercalcemia is surgically corrected. These tumors are histologically distinct fibroosseous lesions without the giant cells seen in "brown tumors." The parathyroid enlargement was mostly uniglandular, with multiple tumors found occasionally. Studies in DNA linkage were performed within this large family and a similar family in Houston to determine if the gene for this syndrome, termed HRPT2, is linked to DNA markers on chromosome 11, to which the gene for multiple endocrine neoplasia (MEN) type 1 has been linked. (This linkage is supported by our findings in one family with MEN 1 reported here.) Linkage studies were also performed with markers on chromosome 10, to which the genes for MEN 2A and MEN 2B have been linked. Evidence against close linkage with chromosome 10 and chromosome 11 markers suggests that this clinically distinct syndrome is also genetically distinct.

Female↗
PubMed1989

Interleukin 3-dependent and -independent mast cells stimulated with IgE and antigen express multiple cytokines.

In response to IgE and specific multivalent antigen, mast cell lines (both growth factor-dependent and -independent) induce the transcription and/or secretion of a number of cytokines having a wide spectrum of activities. We have identified IL-1, IL-3, IL-5, IL-6, IFN-gamma, GM-CSF, JE, MIP1 alpha, MIP1 beta, and TCA3 RNA in at least two of four mast cell clones. The production of these products (except JE) is activation-associated and can be induced by IgE plus antigen. In selected instances cytokine expression can also be induced by activation with Con A or phorbol ester plus ionophore, albeit to levels less than those observed with IgE plus antigen. In addition, long-term mast cell clones and primary cultures of bone marrow-derived mast cells specifically release IL-1, IL-4, and/or IL-6 bioactivity after activation. These findings suggest that in addition to their inflammatory effector function mast cells may serve as a source of growth and regulatory factors. The relationship of mast cells to cells of the T lymphocyte lineage is discussed.

Animals↗
PubMed1989

Cholelithiasis follows total gastrectomy in Zollinger-Ellison syndrome.

The frequent occurrence of cholelithiasis noted in the follow-up of patients who underwent total gastrectomy because of Zollinger-Ellison syndrome prompted us to study this phenomenon. Cholelithiasis is known to be more common after truncal vagotomy, with or without concomitant subtotal gastric resection, and the prevalence of gallstones in these patients is reported to be 16% to 38%. To date, however, no long-term study has investigated the prevalence of gallstones after total gastrectomy in patients with the Zollinger-Ellison syndrome. Since 1961, 26 patients with the Zollinger-Ellison syndrome have undergone total gastrectomy and were enrolled in a Medical College of Wisconsin Clinical Research Center protocol that allowed follow-up to assess the development of cholelithiasis. Eight patients had cholecystectomy at the time of total gastrectomy (seven patients had stones), leaving 18 patients with a normal gallbladder and no gallstones at the time of total gastrectomy. Four patients died early, two of surgical complications, one of tumor progression, and one of alcohol-related trauma. During follow-up, cholelithiasis has developed in 10 of 14 patients (71%) at risk; the mean time to gallstones was 6.3 years (range, 1.2 to 12.9 years). The predictable occurrence of cholelithiasis after total gastrectomy in patients with the Zollinger-Ellison syndrome suggests that cholecystectomy should be performed at the time of total gastrectomy.

Adult↗
PubMed1989

Prospective comparison of radionuclide, computed tomographic, sonographic, and magnetic resonance localization of parathyroid tumors.

The appropriate choice of imaging techniques to localize parathyroid tumors preoperatively remains controversial. We report the first prospective, blinded study to compare the efficacy of four imaging modalities in 100 patients with primary hyperparathyroidism (pHPT). Patients were examined by computer-assisted thallium 201/technetium 99m subtraction scintigraphy (TTS), computed tomography (CT), ultrasonography (US), and magnetic resonance (MR). Each study was performed and interpreted independently. Subsequent neck exploration and "curative" parathyroidectomy allowed correlation of surgical findings with imaging reports to score their accuracy. Overall sensitivities of the four imaging modalities were TTS, 73%, CT, 68%, US, 55%; and MR, 57%; with respective specificities of 94%, 92%, 95%, and 87%. Sensitivities for lesions located below the thyroid gland (thymic tongue and mediastinum) were TTS, 90%; CT, 46%; US, 44%; and MR, 50%; with respective specificities of 100%, 99%, 100%, and 94%. There was a significant increase in overall sensitivity when TTS and CT (90%, p less than 0.01) or TTS and US (85%, p less than 0.05) were used together; however, the combination of any three or even four imaging modalities did not increase sensitivity further. For small parathyroid tumors (less than or equal to 250 mg), no imaging technique had a sensitivity of more than 50%. None of the imaging studies accurately localized small hyperplastic parathyroid glands found in patients with multiple gland disease. Preoperative parathyroid imaging may not be indicated in pHPT patients undergoing first-time neck exploration because surgeons experienced in parathyroid surgery have a 93% to 96% cure rate.

Adult↗
PubMed1988

The expression and regulation of a potential lymphokine gene (TCA3) in CD4 and CD8 T cell clones.

The TCA3 gene was originally isolated from a cDNA library derived from a TH1 (inflammatory) T cell clone. Expression of TCA3 RNA was limited to cells in the activated state. Based on its expression profile and the existence of a hydrophobic leader sequence with a predicted cleavage site, we proposed that TCA3 encodes a new lymphokine. In the present study, we examine the subset distribution, kinetics, and regulation of TCA3 RNA expression. We show that TCA3 is expressed in response to selected T cell-activating stimuli. TCA3 is transcribed to peak steady state levels by 4 h after stimulation in TH1, TH2 (helper), and CTL clones. Two intracellular signals, supplied in vitro by phorbol ester and one of several agents capable of increasing intracellular free calcium concentrations, are required for the initiation of TCA3 transcription. In addition, TCA3 transcription is blocked by anti-L3T4 mAb, suggesting that prior signaling through L3T4 can inhibit expression of TCA3 and other lymphokines. In contrast to IL-2, IL-4, and IFN-gamma TCA3 is uniformly expressed at high levels among all individual T cell clones examined, including four TH1, three TH2, and three CTL clones. Furthermore, activation-specific TCA3 expression can be dissociated from T cell proliferation.

Animals↗
PubMed1988

DNA content in radiation-associated thyroid cancer.

DNA content has been reported to be of prognostic significance in differentiated thyroid carcinoma. Since malignant tumors with irradiation as an initiator often contain DNA aberrations, the DNA content of well-differentiated thyroid carcinoma in patients with a prior history of low-dose head and neck irradiation was determined and compared with similar nonradiation-associated lesions. The DNA content of thyroid cancers from 53 patients was determined with use of flow cytometry. Sixteen radiation-associated thyroid carcinomas (11 papillary, 3 follicular, and 2 medullary) all were diploid. In a group of 37 nonradiation-associated tumors, 10 were aneuploid (10 of 29 papillary carcinomas and 0 of 2 follicular or 6 medullary carcinomas). This difference in DNA content is significant (p less than 0.02, Fisher's exact test). These findings were unexpected and suggest that if the initiating irradiation causes a DNA aberration, this aberration is not reflected in DNA content as measured by means of flow cytometry.

Adenocarcinoma↗
PubMed1987

Cloning and characterization of a novel T cell activation gene.

We have used the technique of subtractive hybridization to identify a T cell gene selectively expressed during activation via the antigen-receptor pathway. This gene, termed TCA3 (for T cell activation) encodes a mRNA which is expressed following concanavalin A (Con A) activation of T cell clones at levels of approximately 1% total poly(A)-containing mRNA. The cDNA isolate, termed TCA3.0, is 512 bases in length excluding poly(A) and encodes a predicted 92-amino acid protein having the characteristics of a secreted polypeptide of approximately 69 amino acids. The genomic organizations of TCA3 was determined for two lambda phage clones and was found to be a single copy gene containing at least three exons dispersed over less than 4.7 kb. The temporal appearance of TCA3 mRNA in response to several activating agents was examined. It is not transcribed in response to interleukin 2 stimulation, but is transcribed in response to either antigen or Con A stimulation and can be detected as early as 1 hr poststimulation. Expression TCA3 in response to Con A is blocked by cyclosporin A treatment. The combined data suggest that TCA3 may represent a new lymphokine.

Amino Acid Sequence↗
PubMed1987

Enlarged parathyroid glands: high-resolution local coil MR imaging.

Twenty-two patients with primary hyperparathyroidism underwent high-resolution magnetic resonance (MR) imaging with local (surface) coils for preoperative localization of enlarged parathyroid glands. The MR studies were interpreted prospectively and the results compared with findings at surgery and the results of computed tomography (CT), ultrasonography (US), and thallium-technetium scintigraphy (TTS). The sensitivity and specificity of MR imaging were .74 and .88, respectively. The sensitivity/specificity for the other modalities were as follows: 74/.95 for CT, .59/.82 for US, and .82/.98 for TTS. Enlarged parathyroid glands displayed a medium-intensity signal on T1-weighted images and a marked increase in intensity on T2-weighted images, but the degree of increase varied considerably.

Adenoma↗
PubMed1987

The effect of parathyroidectomy on the recurrence of nephrolithiasis.

Little information is available on the long-term influence of parathyroidectomy on the rate of renal stone formation in patients with primary hyperparathyroidism (pHPT) and nephrolithiasis. The reported occurrence of renal stone disease in untreated patients with pHPT is 15% to 30%. A registry of 258 pHPT patients who underwent parathyroidectomies at the Milwaukee Regional Medical Center has allowed continued follow-up of the 71 (28%) pHPT patients with associated renal stone disease. Patients have been followed up for an average of 5 years (range, 1 to 15 years) since surgery. The rate of renal stone formation before and after parathyroidectomy was compared. Identification of a "new" renal stone was defined as passage and collection, extraction, or radiographic visualization of stones. All 71 pHPT patients with stone disease had hypercalcemia and inappropriately elevated parathyroid hormone concentrations, and after parathyroidectomy these values returned to normal in 69 of 71 patients. Since undergoing parathyroidectomy, only 4 patients have passed renal stones. The rate of stone formation per patient per year was 0.36 before and 0.02 after surgery (p less than 0.001). Surgical correction of pHPT significantly reduced the rate of stone formation.

Adult↗
PubMed1986

Pancreaticobiliary involvement in familial polyposis coli/Gardner's syndrome.

Adenomatous lesions and carcinoma of the upper gastrointestinal tract, biliary tree, and gallbladder are being reported with increasing frequency in patients with familial polyposis coli or Gardner's syndrome (FPC/GS). A patient with FPC/GS who developed polyps with carcinoma in situ of the common bile duct and ampulla of Vater, along with extensive adenomatous changes in the duodenum, gallbladder, extrahepatic bile ducts, and main pancreatic duct is presented. Proliferative lesions, adenomas, and carcinomas should always be considered in the differential in patients with FPC/GS who have symptoms of upper gastrointestinal, biliary or pancreatic disease.

Biliary Tract↗
PubMed1986

Effect of nitrous oxide inactivation of vitamin B12 on the levels of folate coenzymes in rat bone marrow, kidney, brain, and liver.

The effects of nitrous oxide inactivation of the vitamin B12-dependent enzyme, methionine synthetase, on the distribution of folic acid derivatives in rat bone marrow cells, kidney, brain, and liver were determined. Methionine synthetase activity was decreased by about 90% in bone marrow cells, kidney, and brain and by 83% in liver. The proportion of 5-methyltetrahydrofolate (5-CH3-H4PteGlu) in N2O-exposed rats increased from 1.4- to 1.9-fold depending on the tissue examined. This increase was at the expense of a decrease in different folate derivatives in different tissues--in bone marrow cells, kidney, and liver 5-HCO-H4PteGlu, 10-HCO-H4PteGlu, and H4PteGlu decreased; in brain only H4PteGlu decreased significantly. Total endogenous folates, as measured by Lactobacillus casei after conjugase treatment, were unchanged in all tissues after nitrous oxide exposure. The results are interpreted as direct support of the methyl trap hypothesis as the explanation of the interrelationship of folate and vitamin B12 metabolism in bone marrow cells, kidney, and brain, as well as in liver.

5-Methyltetrahydrofolate-Homocysteine S-Methyltran↗